Evidence map›Paper›PMID 20952679›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

Impaired apoptotic cell clearance in the germinal center by Mer-deficient tingible body macrophages leads to enhanced antibody-forming cell and germinal center responses.

Ziaur S M Rahman, Wen-Hai Shao, Tahsin N Khan, Yuxuan Zhen, Philip L Cohen

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

  1. Pooled it
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  15. Article
  16. Article
  17. Article
  18. Germinal Centre Shutdown.Frontiers in immunology · 2021
    Review
  19. Article
  20. Funerals and Feasts: The Immunological Rites of Cell Death.The Yale journal of biology and medicine · 2019
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Ziaur S M RahmanDepartment of Microbiology and Immunology, Thomas Jefferson University, Philadelphia, PA 19107-5541, USA. zrahman@mail.jci.tju.edu
Wen-Hai Shao
Tahsin N Khan
Yuxuan Zhen
Philip L Cohen
Temple University · USThomas Jefferson University · US

Funding

B Cells in Murine Sjogren's SyndromeR01DE017590 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI COHEN, PHILIP L · 2006 to 2010
$2.4M
Impact of lupus susceptibility loci on peripheral tolerance and onset of diseaseR03AR055701 · NIAMS · THOMAS JEFFERSON UNIVERSITY · PI RAHMAN, ZIAUR · 2008 to 2010
$231k
NIAMS NIH HHS AR055701NIAMS NIH HHS R03 AR055701NIDCR NIH HHS R01 DE017590NIDCR NIH HHS R01DE017590
6 · The paper itself

Abstract

Germinal centers (GCs) are specialized microenvironments that generate high-affinity Ab-forming cells (AFCs) and memory B cells. Many B cells undergo apoptosis during B cell clonal selection in GCs. Although the factors that regulate the AFC and GC responses are not precisely understood, it is widely believed that dysregulated AFCs and GCs contribute to autoimmunity. The Mer receptor tyrosine kinase (Mer) facilitates macrophage clearance of apoptotic cells. The Tyro-3, Axl, and Mer receptors, including Mer, suppress TLRs and cytokine-mediated inflammatory responses. We report in this study that tingible body macrophages (TBMφs) in GCs express Mer. Compared to C57BL/6 (B6) controls, Mer-deficient (Mer(-/-)) mice had significantly higher AFC, GC, and Th1-skewed IgG2 Ab (especially IgG2c) responses against the T cell-dependent Ag (4-hydroxy-3-nitrophenyl) acetyl-chicken γ globulin. Mer(-/-) mice had a significantly higher percentage of GC B cells on days 9, 14, and 21 postimmunization compared with B6 controls. Significantly increased numbers of apoptotic cells accumulated in Mer(-/-) GCs than in B6 GCs, whereas the number of TBMφs remained similar in both strains. Our data are the first, to our knowledge, to demonstrate a critical role for Mer in GC apoptotic cell clearance by TBMφs and have interesting implications for Mer in the regulation of B cell tolerance operative in the AFC and GC pathways.

Indexed as

AnimalsAntibody FormationAntibody-Producing CellsApoptosisCell Separationc-Mer Tyrosine KinaseEnzyme-Linked Immunosorbent AssayFlow CytometryGerminal CenterImmunohistochemistryIn Situ Nick-End LabelingMacrophagesMiceMice, Inbred C57BLMice, KnockoutProto-Oncogene Proteinsc-Mer Tyrosine KinaseMertk protein, mouseProto-Oncogene ProteinsReceptor Protein-Tyrosine Kinases

Identifiers

PMID20952679
PMCPMC3563244
OpenAlexW2123901710

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.